The overall hypothesis of this study is that bronchopulmonary dysplasia (BPD) is the result of injury and abnormal repair to an immature lung. We hypothesize that factors involved in the pathogenesis of BPD include abnormalities (congenital or acquired) of the surfactant proteins, oxidative stress, inflammation and cytokine production leading to pulmonary fibrosis and hypertension with vascular remodeling. Specifically, we propose that transforming growth factor b (TGFb) is a key mediator of inflammation and fibrosis in the premature lung through inhibition of surfactant production and stimulation of matrix constituents. AIM 1: To create a Clinical Data Base and Tissue Bank from premature neonates with lung disease, some of whom will progress to the development of BPD. The broad clinical database, along with biostatistical support, will allow basic science investigators in the SCOR project (Pathobiology of Lung Development and BPD) to test for associations between biochemical parameters and pathogenesis of BPD, as well as possible therapeutic interventions. AIM 2: To determine whether the level of developmental deficiencies of surfactant proteins (SP-A, -B and -C) contribute to the occurrence of BPD. AIM 3: To measure the temporal changes in critical components of the inflammatory process (inflammatory cell composition, inducible nitric oxide synthase (iNOS), plasma nitrotyrosine levels, hyaluronan (HA), and Receptor for HA-mediated motility (RHAMM), and selected cytokines and vasoactive factors) in tracheal aspirate (TA), blood, and urine samples obtained from intubated infants with lung disease, and to correlate these changes with their clinical course.